A reversible tinnitus and hearing loss have long been known to result from large doses of salicylate. Cochlear electrophysiology and otoacoustic emission studies suggest that the drug may interfere with outer hair cell electromotility. Exposure of isolated outer hair cells to sodium salicylate concentrations ranging from 0.05 to 10 mM reveals a dose dependent, reversible loss of turgidity and dimunition of electromotility. There was also a change in membrane conductance with salicylate superfusion that occurred later in time from the onset of shape and electromotility changes. There was no evidence of dose dependence for the change in membrane conductance, nor was the change reversible. The changes in shape and electromotility that we observe in vitro may impair cochlear partition movements in vivo and could account, at least in part, for the salicylate-induced hearing loss and effects on otoacoustic emissions.
Isolated cochlear outer hair cells undergo rapid, force-generating length changes in response to electrical stimulation. The cellular mechanism responsible for electromotility and its structural substrate is not yet known. Salicylates reduce and block electromotility in vitro. Therefore, we exposed isolated outer hair cells from the guinea pig cochlea to various doses of sodium salicylate and evaluated both ultrastructural changes and responses to electrical stimulation. Following salicylate superfusion, the subsurface cisternae showed dilatation, vesiculation and a deviation from their normal, unfenestrated, axial orientation below the plasma membrane. These changes were time and dose dependent and reversible over a time course of about 30 min. Electromotility was blocked and showed recovery following the same time course as the salicylate-induced reversible structural changes. These results indicate that intact, unfenestrated subsurface cisternae are required for the optimal generation of electrically-induced motility in mammalian outer hair cells.
Carcinoid tumors belong to the group of neuroendocrine tumors of epithelial origin, i.e., neuroendocrine carcinomas. These neoplasms usually occur in the gastrointestinal tract or bronchial system but are very rare neoplasms in the larynx. Since carcinoid tumors in this latter site may appear to be undifferentiated by light microscopy, they may possibly be misinterpreted and their neuroendocrine characteristics may remain unrecognized. Using immunohistochemical methods, three carcinoid tumors were studied and showed positive immunostaining for markers of epithelial origin (cytokeratins, epithelial membrane antigen, carcino-embryonic antigen) and, in particular, for markers of neuroendocrine differentiation (chromogranin, synaptophysin, neuron-specific enolase). All tumors expressed calcitonin-, serotonin- and adrenocorticotropic-hormone-like immunoreactivity. In contrast, three poorly differentiated squamous cell carcinomas showed positive immunostaining for epithelial markers but did not show any immunoreactivity with markers of endocrine characteristics. Fine structurally, carcinoid tumor cells contained neurosecretory-type granules scattered throughout the cytoplasm. The present study demonstrated that (1) carcinoid tumors of the larynx possess distinct immunohistochemical characteristics that allow a clear classification, (2) it is advisable to use a battery of primary antibodies rather than rely on specificity and sensitivity of a single marker to establish diagnosis and (3) the fine structural demonstration of neurosecretory-type granules serves as a reliable adjunct to diagnosis.
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